Answers are grounded in this paper and cite their sources.
Mode of action of FC was compared with that of auxin in different experimental systems and the following results were obtained. FC, as well as auxin, primarily induced elongation of the epidermis of pea epicotyl segments, but it also promoted elongation of the inner tissue, as judged by its action in split stem tests, elongation of hollow-cylinder segments and elongation of unpeeled and peeled segments. FC decreased the minimum stress relaxation time (T0) and increased the extensibility (mm/gr) of the epidermal cell wall of pea epicotyl segments, as did auxin. FC failed to induce expansion growth of Jerusalem artichoke tuber slices when given alone or in combination with kinetin or gibberellic acid. FC at concentrations lower than 10−6M, when given with auxin at concentrations lower than 0.03 mg/liter, promoted elongation of Avena coleoptile segments in an additive manner, to achieve the maximum elongation at higher concentrations. An antiauxin, 2,4,6-trichlorophenoxyacetic acid, inhibited the elongation of Avena coleoptile segments due to auxin but not that due to FC. Nojirimycin, an inhibitor of β-glycosidases, inhibited elongation of pea internode segments due not only to auxin but also to FC. At concentrations more than 10−5M FC promoted root elongation of intact lettuce seedlings, which was inhibited by exogenous auxin. From these results it is concluded that FC and auxin have a common mechanism, which may involve hydrogen ion extrusion, leading to cell wall loosening and thus cell elongation. This growth is limited to the extent that the cells are capable of elongating in response to hydrogen ions. Otherwise there is a definite difference in the mode of actions between FC and auxin, including the nature of cellular receptors for these two compounds.
No takes yet. Share an insight, caveat, or question.
Yamagata et al. (1975) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: